Effect of mangiferin on mitochondrial energy production in experimentally induced myocardial infarcted rats

Mangiferin, from the leaves of Mangifera indica Linn., has been suggested as useful in the treatment of cardiovascular disorders. In the present study this drug was examined on the alteration of cardiac energy metabolism in isoproterenol (ISPH) administered myocardial infarcted rats. ISPH (20 mg/kg b.w.), which was administered s.c. twice at an interval of 24 h, caused a significant decrease in the activities of TCA cycle enzymes and antioxidant defense enzymes with a concomitant increase in the lipid peroxidation of heart mitochondria in rat model. The ATP production and the oxidation of succinate in State 3 and 4 decreased significantly in the cardiac mitochondria of ISPH administered rats. These functional alterations were supported by severe modifications in mitochondrial ultrastructure. Pretreatment with mangiferin (100 mg/kg b.w. i.p.) for 28 days prevented these mitochondrial alterations, oxidation with energy metabolism and restored the TCA cycle enzyme activities to near normal values following ISPH administration. The structural integrity of the heart was protected by mangiferin in ISPH administered rats when compared to the untreated controls. The present findings suggest that the protective effect of mangiferin can be attributed to its reducing effect on oxidative damage and activation of mitochondrial energy metabolism. These results could be useful to study and understand the cellular events involved in this cardioprotective mechanism of mangiferin. Our studies of mangiferin on heart failure may have important implication for future therapeutic approaches involving in the prevention of cardiovascular diseases.